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A CARB-funded animal research project by UC Davis researchers suggests that simultaneous exposure to UFPM and O3 increases toxic effects, resulting in stronger responses than expected from either exposure to O3 or UFPM alone. This is the first study to provide direct evidence of UFPM and O3 exposure-induced myocardial injury (heart injury) in an animal model. Using an adult rat model of cardiovascular disease (CVD), this work adds important scientific understanding of the adverse health effects of simultaneous combined-pollutant exposure and provides important insight into the association between ambient air pollution and increased cardiac morbidity and mortality. Please join us for a research seminar to hear an update on UC Davis’s research project that highlights public health impacts of simultaneous exposure to UFPM and O3.
Date: March 10, 2022
Time: 2:00 p.m. – 3:30 p.m.
Location: Webinar
Background
Older individuals with pre-existing cardiovascular disease (CVD) are more susceptible to air pollution, and at greater risk for cardiovascular (CV) events, including stroke, myocardial ischemia, infarction, and sudden death following short-term exposure to air pollutants. Previous studies have consistently demonstrated that exposure to particulate matter 2.5 µm or less in diameter (PM2.5) is associated with increased CV morbidity and mortality, especially in individuals with underlying CVD. Short-term (acute) PM2.5 exposures have been associated with excess CV-related hospitalizations and deaths from myocardial ischemia, heart failure, and arrhythmias. It has also been proposed that ultrafine particulate matter (UFPM) 0.1 µm or less in diameter have greater adverse CV effects due to their large reactive surface area, high particle number counts, and their ability to penetrate the alveoli and translocate into the vasculature. Epidemiologic research has suggested a statistical correlation between exposure to PM2.5 or less in diameter and ozone (O3), and adverse health effects. However, there are few experimental data that support the biological plausibility of the combined effects of these pollutants.
The current study on CVD risk factors in animal lung and heart tissues was undertaken to extend the observations in a previous CARB funded research project that examined the cardio-pulmonary pathophysiological responses of mature adult rats with and without preexisting CVD. This study shows that cardiac fibrosis is significantly greater in mature adult rats exposed to UFPM+O3 compared to rats without cardiovascular diseases.
Speaker Biography
Edward Schelegle, Ph.D., is the Department Chair and Professor of Anatomy, Physiology and Cell Biology in the School of Veterinary Medicine, UC Davis. He received a Bachelor of Science degree in Animal Physiology, a Master of Arts in Physical Education, and a PhD in Physiology from UC Davis. He is also a Core Scientist in the Respiratory Diseases Unit at the California National Primate Research Center, UC Davis. He directs a translational program that examines how environmental factors affect human lung health. His primary research interest is pulmonary neurophysiology with a focus on the role that lung vagal afferents play in the control of breathing, epithelial injury, inflammation, and repair in models of acute and chronic lung injury and/or disease. In addition, he has multiple publications examining the factors that contribute to the exposure-response of ozone in humans.
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